Nephrotoxicity In Wistar Rats Research Articles

Adiantum capillus attained selenium nanoparticles (SeNPs) ameliorate resistive effects in rat model of gentamicin nephrontoxicity via regulation of Interlukin-1β, tumor necrosis factor-α and engagement of Vimentin and Bcl-2 proteins

In this study the green method for synthesizing selenium nanoparticles (SeNPs) is experienced, in which the leaf extract of Adiantum capillus was used as an effective chelating and capping agent for producing SeNPs. The characterization techniques that achieved to confirm the synthesis and the structure details of the SeNPs were: UV–Vis spectroscopy, FT-IR analysis, XRD, EDX and SEM analysis. The biological activity of the synthesized SeNPs were tested and compared to the crude extract of Adiantum capillus on gentamicin model of nephrotoxicity in Wistar rats. Sera were used to test the pro-inflammatory cytokines Tumor necrosis factor alpha (TNF-α) and Interleukin beta (IL-β) levels. Histopathology and immunohistochemistry analysis for the apoptosis regulator protein (Bcl-2) and the interstitial filament protein (Vimentin) were performed. Results revealed that the synthesized SeNPs peak appeared at 400–430 nm wave length with crystallite particle size is around 37 nm. The predominant shape is spherical and cubic at different magnification levels with a narrow size distribution of 22.04–128.43 nm. The synthesized SeNPs showed a strong protective effect against gentamicin induced toxic effects to the rat’s kidneys obtained from the (kidney function parameters, histopathology evaluation, recovery of the pro-inflammatory cytokines IL-β and TNF-α level with retrieval of Bcl-2 and vimentin protein levels proximate to the vehicle control groups). Due to the significant protective effect of SeNPs, it considered much better than the crude extract of Adiantum capillus in the treatment of kidney injury; however, additional studies are necessary to find the precise mechanism of their action.

Ameliorative Effects of Propolis and Royal Jelly against CCl4 -Induced Hepatotoxicity and Nephrotoxicity in Wistar Rats.

Carbon tetrachloride (CCl4 ) is known to have hepatotoxic and nephrotoxic effects. During the two-month CCl4 exposure of Wistar rats, propolis extract (PE) and royal jelly (RJ) were added in order to test the potential protective effect against hepato-renal injury. Ketonuria, proteinuria, high creatinine and urea levels are the result of CCl4 -induced nephrotoxicity. Severe disorders of hematological indicators indicate anemia; high values of leukocytes indicate inflammatory condition. Cytogenetic impairments in hepatocytes, aggregation of platelets, and hypoproteinemia indicate severe liver impairment. Results suggest a more significant protective role of RJ compared to PE. Both extracts regulated proteinuria, ketonuria, hypoproteinemia and reduced platelet aggregation in the hepatic circulation. The increase in the number of erythrocytes (RBC) suggest protective effects against anemia; the decrease in the number of leukocytes can be linked to anti-inflammatory effects. PE and RJ have a beneficial effect against hepato-renal injury, anemia and anti-inflammatory conditions caused by CCl4 .

Ameliorative effect of chitosan nanoparticles against carbon tetrachloride-induced nephrotoxicity in Wistar rats

Context Chitosan is a biocompatible polysaccharide that has been widely exploited in biomedical and drug delivery applications. Objective This study explores the renoprotective effect of chitosan nanoparticles in vivo in rats. Materials and methods Chitosan nanoparticles were prepared via ionotropic gelation method, and several in vitro characterizations were performed, including measurements of particle size, zeta potential, polydispersity index, Fourier transform-infrared spectroscopy, differential scanning calorimetry, and transmission electron microscopy (TEM) imaging. Wistar rats were divided randomly into four groups; negative control, CCl4-induced nephrotoxicity (untreated), and two groups receiving CCl4 + chitosan NPs (10 and 20 mg/kg) orally for 2 weeks. The renoprotective effect was assessed by measuring oxidative, apoptotic, and inflammatory biomarkers, and via histopathological and immunohistochemical examinations for the visualization of NF-κB and COX-2 in renal tissues. Results Monodisperse spherical nanosized (56 nm) particles were successfully prepared as evidenced by dynamic light scattering and TEM. Oral administration of chitosan nanoparticles (10 and 20 mg/kg) concurrently with CCl4 for 2 weeks resulted in 13.6% and 21.5% reduction in serum creatinine and increase in the level of depleted reduced glutathione (23.1% and 31.8%), respectively, when compared with the positive control group. Chitosan nanoparticles (20 mg/kg) revealed a significant (p ˂ 0.05) decrease in malondialdehyde levels (30.6%), tumour necrosis factor-α (33.6%), interleukin-1β (31.1%), and caspase-3 (36.6%). Conclusions Chitosan nanoparticles afforded significant protection and amelioration against CCl4-induced nephrotoxicity. Thus, chitosan nanoparticles could afford a potential nanotherapeutic system for the management of nephrotoxicity which allows for broadening their role in biomedical delivery applications.

Gallic and Hesperidin Ameliorate Electrolyte Imbalances in AlCl3-Induced Nephrotoxicity in Wistar Rats.

Nephrotoxicity is usually characterized by inefficiency of the kidney, thereby causing disruptions to electrolyte balance and blood acidity. This study aimed to evaluate the effect of hesperidin and gallic acid on serum electrolytes and ion pumps in Wistar rats subjected to aluminum chloride (AlCl3)-induced nephrotoxicity. Thirty Wistar rats were randomly divided into six groups of five animals apiece. Group one served as the negative control and received distilled water while the study lasted. Animals in groups 2–4 received 100 mg/kg/day AlCl3 throughout the study. Animals in groups 3 and 4 were also administered 100 mg/kg/day gallic acid and 100 mg/kg/day hesperidin, respectively. Groups 5 and 6 were treated with 100 mg/kg/day gallic acid only and 100 mg/kg/day hesperidin only, respectively. Treatments were administered orally via gavage for 28 days with distilled water as the vehicle. Animals were sacrificed after which levels of potassium, calcium, magnesium, phosphate, chloride, and bicarbonate ions were evaluated in the serum, while activities of Na+/K+ and Ca2+/Mg2+ ATPases were determined in kidney homogenate. Results showed that AlCl3 significantly (p < 0.05) inhibited activities of Na+/K+ and Ca2+/Mg2+ ATPases in addition to increasing serum levels of potassium, calcium, phosphate, and chloride, with concomitant decrease in serum levels of magnesium and bicarbonate. However, coadministration of AlCl3 with either gallic acid or hesperidin ameliorated all the disruptions caused by AlCl3. It could be concluded that gallic acid and hesperidin could be relevant in managing electrolyte imbalances and acidosis occasioned by kidney dysfunction.

Protective effects of metformin against aluminum phosphide-induced acute hepato-renal damage in rats: An experimental approach

Phosphine (PH3), from hydrolysis of magnesium, zinc, and aluminum phosphide (AlP), is a rodenticide and insecticide which is used to avoid losses of the agriculture products. However, using of this agent may affect the human health, in a way that poisoning with AlP has a high rate of mortality and morbidities. This study determined the ameliorative effects of metformin (MET) on AlP-induced hepato- and nephro-toxicity in Wistar rats. Male rats were randomly divided into four experimental groups. Group I was the control group received coconut oil by oral gavage, group II was the model group received AlP (12 mg/kg) distributed in coconut oil by oral gavage, group III received MET (200 mg/kg; i.p.), and group IV received MET (200 mg/kg; i.p.) 30 min after intoxication. After 24 h, the serum, liver and kidney tissues were collected for histopathological and biochemical investigations. The levels of kidney function markers, blood urea nitrogen and creatinine, and liver function markers, ALP, AST and ALT, in the plasma were increased significantly followed by AlP intoxication. The results revealed that phosphine causes a significant enhancement of lipid peroxidation, while decreases the activity of superoxide dismutase in both liver and kidney tissues. Furthermore, phosphine significantly induced the up-regulation of TNF-α and phosphorylation of NF-κB in target tissues. Overall, treatment with MET abolished aforementioned alterations resulted by AlP intoxication. Furthermore, histological evaluation indicated a deleterious effect of AlP on the liver and kidney tissues along with marked increase in kidney and liver injury scores, which is mitigated by MET administration. According to our results, although metformin could not bring the changes to the level of the control group, it was indicated that this drug might possess a protective effect against AlP-induced hepato and nephrotoxicity by inhibiting inflammatory responses and oxidative stress.

Metabolite Profiling and Nephroprotective Potential of the Zea mays L. Silk Extract against Diclofenac-Induced Nephrotoxicity in Wistar Rats.

The lack of sufficient scientific evidence prompted the analytical investigation of nephroprotective potential of the silk extract of Zea mays L., which is traditionally and ethnomedicinally used for various disorders including kidney dysfunction. The present study was conducted to investigate the phytochemical analysis and demonstrate the nephroprotective potential of the methanolic silk extract of Z. mays L. using a rodent model. High-performance thin-layer chromatography (HPTLC) analysis was carried out to standardize the methanolic silk extract of Z. mays (ZME) using naringenin as a marker. The metabolite profiling of the ZME was carried out using ultrahigh-performance liquid chromatography mass spectrometry (UPLC-MS) on a monolithic capillary silica-based C18 column to identify bioactive compounds and for confirmation of the identified markers. Furthermore, for acute toxicity study, a single dose (2000 mg/kg bw) of the ZME was administered orally to Wistar rats. Also, nephrotoxicity was induced in Wistar rats by injecting diclofenac (DC) (50 mg/kg, bw, i.p.) at a single dose. The efficacy of the ZME as a nephroprotective agent was then evaluated at doses of 100, 200, and 400 mg/kg/day, bw, p.o. Furthermore, the kidney, liver, antioxidant, inflammatory, and apoptotic biochemical markers and histopathological and immunohistochemical alterations (caspase-3 and reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-4 (NOX-4)) were evaluated. Phytochemical analysis by HPTLC and UPLC-MS revealed the presence of naringenin, vanillic acid, ferulic acid, gallic acid (GA), ellagic acid, quercetin, and morin, along with other bioactive constituents exhibiting multiple pharmacological properties. The acute toxicity study of the ZME showed no mortality or any clinical signs of toxicity through all the 14 days of the toxicity study at a dose of 2000 mg/kg. Also, administration of DC caused a significant elevation (P < 0.001) in kidney biochemical parameters and also caused oxidative, inflammatory, and apoptotic stress. Furthermore, DC also caused histopathological and immunohistochemical changes. Pretreatment with the ZME attenuated the elevated biochemical markers significantly at medium and high doses along with improvement in histopathological and immunohistochemical damages and showing comparable results to those of α-ketoanalogue. The present study verifies the traditional claims of Z. mays silk alleviating various kidney and related disorders by concluding the nephroprotective potential of the ZME. The nephroprotective activity of the ZME is attributed to the phytoconstituents present, acting as potent restoring antioxidants and preventing inflammatory and apoptotic cellular damages in rats. Thus, it holds promising potential in the management of nephrotoxicity.

Nephroprotective Effects of Polyherbal Formulation on Gentamicin-induced Toxicity in Wistar Rats

Effect of a polyherbal formulation (polyherbal alcoholic extract; PAE) prepared from Withania somnifera (root), Aegle marmelos (leaves), Tribulus terrestris (fruit) was studied on gentamicin-induced nephrotoxicity. Thirty Wistar rats were equally divided into five groups; group I (control), group II (gentamicin alone), group III (prophylactic), group IV (curative) and group V (formulation alone). Gentamicin caused signs of depression, dullness, polyurea, restlessness, reduced body weight, and reduced water and feed intake. These toxicity signs were recovered in the PAE pre-treated prophylactic group; however, in the PAE-treated therapeutic group, some mild toxicity signs were noticed and subsided gradually. Gentamicin increased relative kidney weight but in groups III and IV animals, no significant effect was observed. The Hb, PCV, TEC, TLC and MCV of group II animals revealed a significant decrease, whereas; BUN, creatinine, AST, ALT, ALP, total protein, albumin and globulin were significantly increased. The PAE treatment caused significant recovery in these hematobiochemical parameters in groups III and IV. Gentamicin caused histopathological alterations in kidney represented by focal renal degenerative and necrotic changes, with intratubular hyaline cast. In PAE-treated groups III and IV, minimal histopathological alterations were seen. In conclusion, PAE showed significant protective and moderate therapeutic potential against gentamicin-induced nephrotoxicity in Wistar rats.

The protective role of some natural antioxidants against some nanoparticles-induced subchronic nephrotoxicity in Wistar rats

The protective role of some natural antioxidants against some nanoparticles-induced subchronic nephrotoxicity in Wistar rats

Comparative studies on protective efficacy of gentisic acid and 2-pyrocatechuic acid against 5-fluorouracil induced nephrotoxicity in Wistar rats

Nephrotoxicity is a frequent and severe side effect of 5-fluorouracil (5-FU) chemotherapy which limits its use clinically regardless of being one of the most promising chemotherapeutic agents. Here, we assessed the nephroprotective activity of two structurally related phenolic acids 2-pyrocatechuic acid (2,3 dihyroxybenzoic acid) and gentisic acid (2,5 dihyroxybenzoic acid) against 5-FU induced nephrotoxicity in Wistar rats. Intraperitoneal administration of 5-FU at a dose of 20 mg/kg once a day for 5 days produced a significant elevation in serum parameters of the kidney such as uric acid, urea, creatinine, sodium and potassium levels along with severe histopathological changes in renal tissues of rats indicating severe nephrotoxicity. Administration of 2-pyrocatechuic acid (2-PCA) at 10, 30 and 100 by oral route for 9 days and additional 5 days with 5-FU resulted in an amelioration of altered serum parameters in a dose-dependent manner. Moreover, 2-PCA attenuated the renal damage produced by 5-FU demonstrating its efficacy as a nephroprotective agent for the prevention as well as amelioration of 5-FU induced nephrotoxicity. None of the doses of gentisic acid (GA) were found to be effective in this posology when given orally.

Andrographis paniculata mitigates first-line anti-tubercular drugs-induced nephrotoxicity in Wistar rats

Context Anti-tubercular drugs (ATDs) mediated adverse drug reactions are major concerns for clinicians to treat tuberculosis infection. This study aimed to investigate Andrographis paniculata extract-based phytotherapy to combat the nephrotoxic effects caused by ATDs therapy. Methods Reno-protective effect of A. paniculata extract in ATDs-induced rats was evaluated through LPO, GSH, CAT, SOD, GST, urea, creatinine, uric acid, and histopathological studies. Standardization of the extract was performed using RP-HPLC and FTIR analysis. Whereas, the effect of A. paniculata extract on ATDs induced genetic perturbation was analyzed using micronucleus assay. Moreover, the expression level of the xenometabolic gene was investigated using RT-PCR to explore the therapeutic mechanism. Results The nephrotoxic effect of ATDs was indicated by elevated levels of LPO and renal function markers along with the reduced activity of renal antioxidants. An up-regulated expression profile of NAT gene and histological alterations were observed in renal tissue however, micronucleated PCEs were observed in bone marrow cells. Concomitant treatment with A. paniculata extract revealed a noticeable amelioration of elevated oxidative stress markers, gene expression levels, genotoxic perturbation, and histological alterations in a dose-dependent manner. Conclusion Hence, the present study using A. paniculata leaf extract confirmed to play effective phytotherapy against ATDs induced renal toxicity.

Evaluation of protective effect of methanolic leaves extract of Solanum incanum in copper induced nephro-toxicity in wistar rats

Evaluation of protective effect of methanolic leaves extract of Solanum incanum in copper induced nephro-toxicity in wistar rats

Renoprotective effects of Adansonia digitata leaf extract on renal function and histopathological changes in vancomycin-induced nephrotoxicity in Wistar rats

Renoprotective effects of Adansonia digitata leaf extract on renal function and histopathological changes in vancomycin-induced nephrotoxicity in Wistar rats

Protective effect of Geophila obvallata (Shumach) Didr leaf extract and its fractions against cadmium-induced nephrotoxicity in male Wistar rats

Cadmium (Cd) is a known nephro-toxicant. This research determined the ameliorative effects of Geophila obvallata crude methanol extract (Me70) and its fractions on Cd-induced nephrotoxicity in Wistar rats. Male rats were randomly allocated to nine (9) groups of six (6) rats each. Group I was given normal water and feed only. Group II received 0.3 mg Cd/L only for two weeks. Groups III, IV, V, VI and VII were pre-exposed to aqueous, ethyl acetate, hexane, butanol and chloroform fractions of Me70, each at a dose of 50 mg/kg bwt for fourteen (14) days prior to treatment with 0.3 mg Cd/L for a further two weeks. Group VIII was pre-exposed to Me70 at a dose of 50 mg/kg bwt for fourteen (14) days, prior to administration of 0.3 mg Cd/L for fourteen (14) days, while group IX received 50 mg/kg.bwt of Me70 only for fourteen (14) days. The treatments were administered daily for twenty-eight (28) days via oral gavage. Cadmium levels in the kidney tissues of Cd-treated rats increased significantly while their body weights decreased relative to control. The levels of kidney function markers in the plasma, lipid peroxidation levels, catalase activity, metallothionine (MT-1) and kidney injury molecule-1 (KIM-1) mRNA were increased significantly, while glutathione (GSH) levels, activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione-s-transferase (GST), and levels of nuclear factor erythroid-2-related factor 2 (Nrf-2), peroxisome proliferator-activated receptor –gamma coactivator- 1-alpha (PGC-1α), heme oxygenase-1 (HO-1) and NADH quinone oxidoreductase-1 (NQ-O1) were decreased significantly in rats treated with Cd-only. Overall, pre-treatment with Me70 produced better protection from the toxic effects of cadmium induction in experimental rats.

Protective Effect of Celastrus paniculatus Seed Extract against Lead Acetate Induced Nephrotoxicity in Wistar Rats

Protective Effect of Celastrus paniculatus Seed Extract against Lead Acetate Induced Nephrotoxicity in Wistar Rats

The Protective Effect of Vernonia Amygdalina in Lead Acetate-Induced Nephrotoxicity in Wistar Rats

Introduction / Background: Inadvertent poisoning from indiscriminate use of lead acetate-containing agents has transformed into an issue of public health concern, most especially in developing countries, coupled with the paucity of potent antidotes. Aims: We investigated the protective effect of Vernonia amygdalina in lead acetate-induced nephrotoxicity in Wistar rats. Materials and Methods: In this study, thirty adult rats of either sex were divided into five groups of six animals each. Groups A and B were administered (daily) distilled water and lead acetate, respectively for 28 days. Groups C, D, and E received (daily) lead acetate at doses of 100 mg/kg body weight and aqueous extract of V. amygdalina at doses of 100, 200, and 250 mg/kg body weight, respectively, for 28 days. Results: The results from the study showed that were significant (P &lt; 0.05) increases in the levels of serum creatinine, urea, sodium Na + and chloride Cl − in lead-intoxicated rats when compared to the control group. There was significant (P &lt; 0.05) decrease in the serum levels of superoxide dismutase, catalase, peroxidase (GPx) Uric acid, URA and reduced glutathione (GSH) as the consequences of lead acetate administration. The histograms of the rats intoxicated with lead acetate were characterized by tubular necrosis and a reduction in myeloid-erythroid cells. Treatment with aqueous extract of V. amygdalina at the doses of 100, 200, and 250 mg/kg body weight significant (P &lt; 0.05) protected against these alterations. The dose of 250 mg/kg exhibited the highest protective activity. Conclusion: Results of the present study may suggest that V. amygdalina possess a potent phytochemical that could be standardized for use in kidney and other related oxidative damage diseases.

Nephroprotective role of diosgenin in gentamicin-induced renal toxicity: biochemical, antioxidant, immunological and histopathological approach

BackgroundAminoglycoside antibiotics, gentamicin (GM) owns the utmost nephrotoxic potential than other antibiotics from the same category. To the other side, diosgenin (DG) showed the antioxidant and anti-inflammatory property.ResultsThe present study was aimed to explore the nephroprotective effect of diosgenin on gentamicin-induced renal toxicity in Wistar rats. Wistar albino rats were divided into six groups (n = 6): Normal control (NC), Nephrotoxicity control (GM), DG (20 mg/kg), DG (40 mg/kg), DG (80 mg/kg), accordingly. After the treatment, the nephroprotective effects of DG were assessed by measuring serum levels of creatinine (Cr), blood urea nitrogen (BUN), total proteins (TP), albumin and urea levels. Urine volume, proteins, electrolyte levels, creatinine clearance were also evaluated in urine samples. Oxidative stress was evaluated through the measurement of antioxidant stress markers in the kidney tissue. Changes in body weight and kidney weight were also recorded along with a histopathological examination of kidney sections. For evaluation of inflammation, TNF-α and IL-1β levels were measured in the blood serum using ELISA kits. GM intoxication induced elevated serum creatinine, BUN, urea, albumin and TP levels, urine electrolytes levels, pro-inflammatory cytokines, antioxidant parameters which were found to be decreased significantly in a dose-dependent manner in rat groups received DG which was also evidenced by the histological observations.ConclusionDG showed a significant nephroprotective effect in a dose-dependent manner by ameliorating the GM induced nephrotoxicity in Wistar rats.

Nephroprotective and anti-inflammatory potential of aqueous extract from Persea americana seeds against cadmium-induced nephrotoxicity in Wistar rats.

Cadmium is a toxic metal and poses a high environmental risk to animals and humans, alike. It is thus pertinent to search for medicinal plants in protecting against cadmium toxicity. This study aims at investigating the ability of aqueous extract of Persea americana seeds (AEPA) in ameliorating the toxic effects of cadmium in the kidneys of cadmium-exposed Wistar rats. Male Wistar rats were grouped into five, of six animals each. Different groups of animals received normal saline (control group), 200mg/kg body weight AEPA, 400mg/kg AEPA, and standard drug, Livolin Forte, respectively. A last group of animals was left untreated. To induce toxicity, all animals, except the control group, were exposed to cadmium (200mg/L, as CdCl2) in their main drinking water for 21days. Biochemical analysis of serum kidney markers, oxidative stress and antioxidant status, as well as anti-inflammatory activities, was done using standard methods and kits. In silico analysis was performed on phytochemicals reported to be abundant in AEPA. Treatment with 400mg/kg AEPA significantly reversed (P ≤ 0.05) the adverse effect of cadmium on serum creatinine, urea, uric acid and blood urea nitrogen, and restored (P ≤ 0.05) antioxidant status, evidenced by its significant effect on superoxide dismutase, catalase, glutathione-S-transferase, glutathione peroxidase, reduced glutathione, and lipid peroxidation activities. AEPA, at 400mg/kg also exhibited significant anti-inflammatory effects, which was shown by reduced interleukin-2 and tumour necrosis factor α activities. Molecular docking of phytochemicals with the selected protein target also confirmed the therapeutic potential of AEPA. The study concluded that aqueous extract of AEPA protects against cadmium-induced kidney toxicity and inflammation.

Protective effect of propolis from Tigzirt on epirubicin-induced cardiotoxicity and nephrotoxicity

Context: Epirubicin (EPI), belonging to the anthracycline family, is one of the most effective chemo-therapeutic agents used in the treatment of a variety of solid and hematologic malignant tumors but Its anti-tumor efficacy is dose-dependent, but its clinical use is limited by the development of cardiac, hepatic and nephrotic toxicities. Aims: To evaluate the protective effect of ethyl acetate extract of propolis (EAP) native to Tigzirt on selected antioxidant status parameters and biomarkers of epirubicin-induced cardiotoxicity and nephrotoxicity in rats. Methods: Thirty male Wistar albino rats were divided into five groups. It orally dosed with (EAP) or quercetin during 15 days before being subjected to toxicity by injection (i.v) of a cumulative dose of 9 mg/kg of epirubicin to repair cardiac and renal damage. Results: Injection of epirubicin to rats induced cardiac and renal dysfunction as evidenced by a significant increase (P&lt;0.05) in serum levels of biochemical markers (CKmb, BNP, LDH, troponin, urea, creatinine and uric acid). This toxicity thus caused lesions, necrosis, and inflammatory infiltrate in the heart and kidneys. The administration of 250 mg/kg of EAP allowed restoring these functions by lowering the level of these parameters. Thus, a balance of oxidative stress was demonstrated with a decrease of +50% in the level of malondialdehyde and nitric oxide and an increase in superoxide dismutase, catalase and glutathione peroxidase. Therefore, significant restoration was observed on organ architecture. Conclusions: These results show that propolis is rich in phenolic substances, which gave the protective and curative effects against epirubicin-induced cardiotoxicity and nephrotoxicity in Wistar rats.

Curative Effect of Aqueous Seed Extract of Citrus paradisi against Carbon Tetrachloride-Induced Nephrotoxicity in Wistar Rats

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The Effect of Ethanolic Extract of Myrmecodia pendans on Gentamicin Induced Nephrotoxicity in Wistar Rats

The purpose of the study was to investigate the nephroprotective effect of the Myrmecodia pendans extract on Wistar rats. The nephrotoxicity of the animals was induced through intra-peritoneal administration of 100mg/kg/day of gentamicin for ten days. The effect of M. pendans extract at a dose of 250mg/kg/day was concurrently monitored in some rats by assessing their serum creatinine levels, blood urea nitrogen (BUN) and the histopathological parameters. The mean of serum creatinine in control group was 1.17±0.18mg/dl and in nephrotoxic group it was 2.22±0.29 mg/dl, while in group given the extract were 1.38±0.19 and 1.27±0.15mg/dl, respectively. In that group also sequentially showed BUN levels of 24.27±2.6, 108.13±11.58, 30.70±4.23 and 27.28±2.84mg/dl, respectively. Nephrotoxicity was induced in the animals injected with gentamicin, which showed a significant (P&lt;0.05) increase in creatinine and BUN compared with control group. The results also showed that the M. pendans ethanolic extracts significantly (P&lt;0.05) prevented the increase in the levels of serum creatinine, BUN and reduced renal histopathological damage such as hydropic degeneration, vascular congestion and tubular necrosis. Therefore, the ethanolic extract of M. pendans exhibits a nephroprotective activity.